Modulation of the Ca(2+) permeability of human endplate acetylcholine receptor-channel.

Abstract

In slow-channel congenital myasthenic syndrome, point mutations of the endplate acetylcholine receptor (AChR) prolong channel openings, leading to excessive Ca(2+) entry with ensuing endplate degeneration and myasthenic symptoms. The Ca(2+) permeability of the human endplate AChR-channel is quite high, and is further increased by two slow-channel mutations… (More)
DOI: 10.1016/j.ceca.2011.03.002

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